Shock compression of feldspars

Hugoniot data for oligoclase and microcline to 670 and 580 kb and release adiabat data for oligoclase were obtained by means of the inclined mirror and immersed-foil-reflected-light techniques, respectively. Oligoclase and microcline have Hugoniot elastic limits in the range of 40–55 and 80–85 kb. These limits increase slightly with increasing driving shock pressure. Above the elastic limit, extending to ∼300 and ∼400 kb, transition regions of anomalously high compression are observed for microcline and oligoclase. These data and the data of McQueen, Marsh, and Fritz for albitite and anorthosite indicate that at successively higher shock pressures within this region, the feldspars gradually transform to a high-pressure, high-density polymorph. This polymorph probably corresponds to the rutile-like hollandite structure obtained in high-pressure quenching experiments by Kume, Matsumoto, and Koizumi (in KAlGe_3O_8) and by Ringwood, Reid, and Wadsley (in KAlSo_3O_8, microcline). In the hollandite structure germanium or silicon is in octahedral coordination with oxygen. The zero-pressure density and the Birch-Murnaghan equation of state parameters for the adiabat and isotherm are calculated for the high-pressure polymorphs of oligoclase, microcline, anorthosite, and albitite. The release adiabat centered at 180 kb indicates that at this shock pressure some (∼15%) of the hollandite phase forms but apparently reverts to a lower-density phase on pressure release. Release adiabat curves centered at 272 and 417 kb and calculated postshock temperatures indicate that material of feldspar composition recovered from meteorite and laboratory impacts is converted to the hollandite structure upon shock compression; upon pressure release this material probably reverts to the low-density maskelynite form

Metabolic correlates of prevalent mild cognitive impairment and Alzheimer's disease in adults with Down syndrome.

IntroductionDisruption of metabolic function is a recognized feature of late onset Alzheimer's disease (LOAD). We sought to determine whether similar metabolic pathways are implicated in adults with Down syndrome (DS) who have increased risk for Alzheimer's disease (AD).MethodsWe examined peripheral blood from 292 participants with DS who completed baseline assessments in the Alzheimer's Biomarkers Consortium-Down Syndrome (ABC-DS) using untargeted mass spectrometry (MS). Our sample included 38 individuals who met consensus criteria for AD (DS-AD), 43 who met criteria for mild cognitive impairment (DS-MCI), and 211 who were cognitively unaffected and stable (CS).ResultsWe measured relative abundance of 8,805 features using MS and 180 putative metabolites were differentially expressed (DE) among the groups at false discovery rate-corrected q< 0.05. From the DE features, a nine-feature classifier model classified the CS and DS-AD groups with receiver operating characteristic area under the curve (ROC AUC) of 0.86 and a two-feature model classified the DS-MCI and DS-AD groups with ROC AUC of 0.88. Metabolite set enrichment analysis across the three groups suggested alterations in fatty acid and carbohydrate metabolism.DiscussionOur results reveal metabolic alterations in DS-AD that are similar to those seen in LOAD. The pattern of results in this cross-sectional DS cohort suggests a dynamic time course of metabolic dysregulation which evolves with clinical progression from non-demented, to MCI, to AD. Metabolomic markers may be useful for staging progression of DS-AD

Clar Sextet Analysis of Triangular, Rectangular and Honeycomb Graphene Antidot Lattices

Pristine graphene is a semimetal and thus does not have a band gap. By making a nanometer scale periodic array of holes in the graphene sheet a band gap may form; the size of the gap is controllable by adjusting the parameters of the lattice. The hole diameter, hole geometry, lattice geometry and the separation of the holes are parameters that all play an important role in determining the size of the band gap, which, for technological applications, should be at least of the order of tenths of an eV. We investigate four different hole configurations: the rectangular, the triangular, the rotated triangular and the honeycomb lattice. It is found that the lattice geometry plays a crucial role for size of the band gap: the triangular arrangement displays always a sizable gap, while for the other types only particular hole separations lead to a large gap. This observation is explained using Clar sextet theory, and we find that a sufficient condition for a large gap is that the number of sextets exceeds one third of the total number of hexagons in the unit cell. Furthermore, we investigate non-isosceles triangular structures to probe the sensitivity of the gap in triangular lattices to small changes in geometry

Relationship between haemodynamic impairment and collateral blood flow in carotid artery disease

Collateral blood flow plays a pivotal role in steno-occlusive internal carotid artery (ICA) disease to prevent irreversible ischaemic damage. Our aim was to investigate the effect of carotid artery disease upon cerebral perfusion and cerebrovascular reactivity and whether haemodynamic impairment is influenced at brain tissue level by the existence of primary and/or secondary collateral. Eighty-eight patients with steno-occlusive ICA disease and 29 healthy controls underwent MR examination. The presence of collaterals was determined with time-of-flight, two-dimensional phase contrast MRA and territorial arterial spin labeling (ASL) imaging. Cerebral blood flow and cerebrovascular reactivity were assessed with ASL before and after acetazolamide. Cerebral haemodynamics were normal in asymptomatic ICA stenosis patients, as opposed to patients with ICA occlusion, in whom the haemodynamics in both hemispheres were compromised. Haemodynamic impairment in the affected brain region was always present in symptomatic patients. The degree of collateral blood flow was inversely correlated with haemodynamic impairment. Recruitment of secondary collaterals only occurred in symptomatic ICA occlusion patients. In conclusion, both CBF and cerebrovascular reactivity were found to be reduced in symptomatic patients with steno-occlusive ICA disease. The presence of collateral flow is associated with further haemodynamic impairment. Recruitment of secondary collaterals is associated with severe haemodynamic impairment

A review of RCTs in four medical journals to assess the use of imputation to overcome missing data in quality of life outcomes

Background: Randomised controlled trials (RCTs) are perceived as the gold-standard method for evaluating healthcare interventions, and increasingly include quality of life (QoL) measures. The observed results are susceptible to bias if a substantial proportion of outcome data are missing. The review aimed to determine whether imputation was used to deal with missing QoL outcomes. Methods: A random selection of 285 RCTs published during 2005/6 in the British Medical Journal, Lancet, New England Journal of Medicine and Journal of American Medical Association were identified. Results: QoL outcomes were reported in 61 (21%) trials. Six (10%) reported having no missing data, 20 (33%) reported ≤ 10% missing, eleven (18%) 11%–20% missing, and eleven (18%) reported >20% missing. Missingness was unclear in 13 (21%). Missing data were imputed in 19 (31%) of the 61 trials. Imputation was part of the primary analysis in 13 trials, but a sensitivity analysis in six. Last value carried forward was used in 12 trials and multiple imputation in two. Following imputation, the most common analysis method was analysis of covariance (10 trials). Conclusion: The majority of studies did not impute missing data and carried out a complete-case analysis. For those studies that did impute missing data, researchers tended to prefer simpler methods of imputation, despite more sophisticated methods being available.The Health Services Research Unit is funded by the Chief Scientist Office of the Scottish Government Health Directorate. Shona Fielding is also currently funded by the Chief Scientist Office on a Research Training Fellowship (CZF/1/31)